Paradoxical augmentation of (-)Bay K 8644-induced calcium influx by nitrendipine.

(-)Bay K 8644 produced a concentration-dependent contraction of porcine coronary artery rings with the maximal contraction at 10(-6) M. Pretreatment of the rings with 10(-6) M nitrendipine inhibited (-)Bay K 8644-induced contraction, while pretreatment with 10(-8) M nitrendipine potentiated the contraction elicited by (-)Bay K 8644. (-)Bay K 8644 (10(-6) M) significantly stimulated Ca2+ influx. Although 10(-8) M nitrendipine never stimulated Ca2+ influx, Ca2+ influx induced by (-)Bay K 8644 was significantly potentiated by pretreatment with 10(-8) M nitrendipine. Pretreatment with 10(-6) M nitrendipine significantly decreased Ca2+ influx in tissues treated with (-)Bay K 8644. Our results suggest that the increased Ca2+ influx might be involved in the mechanisms by which (-)Bay K 8644-induced contraction was potentiated by pretreatment with nitrendipine.